Outgrowth, extension and coiling are key steps in the development of the cochlear duct. Previous results from our laboratory and others have indicated that an evolutionarily conserved pathway referred to as the planar cell polarity (PCP) pathway plays a role in cochlear outgrowth. However, none of the molecules in the PCP pathway act to generate the molecular force necessary for cochlear outgrowth. Recently, a specific myosin molecule, non-muscle myosin II, has been implicated as an effector of the PCP pathway. Therefore, we sought to determine whether myosin II plays a role in cochlear outgrowth. Localization of the three different Myosin heavy chain genes, Myosin IIA, IIB and IIC, indicated that Myosin IIB and IIC are both expressed in the developing cochlear duct. Moreover, pharmacological inhibition of myosin II in vitro inhibited cochlear outgrowth, indicating that myosin II plays an important role in this event. To confirm the role of myosin II, we expressed a dominant negative version of Myosin IIB exclusively within the developing inner ear. A dominant negative was used because single deletions of either Myosin IIB or IIC had not phenotype as a result of functional compensation between the two genes. Expression of dominant negative Myosin IIB leads to shortened cochleae as a result of defects in the growth of cells within the duct. Ongoing experiments will determined the molecular role of myosin IIs action and the basis for that action in cochlear outgrowth.